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Biomed > BI513 Nervous System > Flashcards

BI513 Nervous System Flashcards

1
Q

What are the 3 classifications of neurons and what do they do?

A

1) Afferent neurons - carry info to CNS
2) Interneurons - integrate info in CNS
3) Efferent neurons - carry info away from CNS

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2
Q

What are the two types of glial cells in the PNS and what are their functions?

A

1) Schwaan Cells - produce myelin
- secrete neurotrophic factors e.g nerve growth factor

2) Satellite Cells - support cell bodies in ganglia

Note: ganglia are clusters of cell bodies outside the CNS

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3
Q

What are the 4 types of glial cells in the CNS and what are their functions?

A

1) Oligodendrocytes - produce myelin
2) Microglia - Macrophage type cells that protect the nerve cells
3) Astrocytes
- secrete neurotrophic factors
- take up neurotransmitters (essential to prevent continued action)
- surround the capillaries that form the blood-brain barrier which regulates movement of substances between blood and brain
- provide neurons with substances for ATP synthesis
4) Ependymal cells
- forms a layer of epithelial cells (the ependyma), that lines the ventricles of the brain and the central canal of the spinal cord
- some act as stem cells that can differentiate into neurons and glia

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4
Q

How much of the axon does each Schwaan cell myelinate?

A

~ 1-1.5 mm

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5
Q

How many layers of myelin can an axon be wrapped in?

A

up to 150

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6
Q

What is white matter?

A

Areas of the CNS that contain high numbers of myelinated axons

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7
Q

What is grey matter?

A

Areas of the CNS that contain a high number of cell bodies, dendrites and unmyelinated axons

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8
Q

What are the 3 types of channels in neuronal membranes?

A

1) Voltage gated
2) Chemical gated
3) Mechanically gated

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9
Q

What are the characteristics of graded potentials

A
  • size of depolarisation or hyperpolarisation is directly proportional to signal strength
  • usually occurs at dendrites and cell bodies
  • two signals arriving close together may sum to produce a larger response
  • if graded potentials are large enough (suprathreshold) they will initiate an action potential
  • potentials lose strength with distance from site of initiation
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10
Q

What are the characteristics of an action potential?

A
  • All or nothing law
  • strength and duration of stimulus represented by frequency of action potentials
  • usually occur at axon hillock
  • no summation due to refractory period
  • permit rapid signalling over long distances
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11
Q

Explain how an action potential occurs

A

1) Resting membrane potential (-70mV)
2) Depolarising stimulus
3) Membrane depolarises to threshold
Voltage gated Na+ channels open
4) Na+ entry further depolarises membrane
5) Voltage gated K+ channels open (+30mV)
6) K+ leaves the cell
Membrane returns to resting potential
7) Cell hyperpolarises due to loss of K+ (-90mV)
8) Voltage gated channels close
9) Resting membrane potential restored by Na+/K+ pump

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12
Q

How does an action potential move along an axon?

A

Positive charge created flows into adjacent region of the axon by local current flow

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13
Q

What 2 physiological factors affect the speed of conduction?

A

1) Axon diameter
- larger diameter + faster speed as less resistance to current flow
2) Myelination
- Saltatory conduction can occur in myelinated axons
- conduction slowed in demyelinated axons

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14
Q

How do myelinated axons allow faster conduction?

A

Current flows from one node of Ranvier to the next through insulated regions of axon which are resistant to current leak

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15
Q

How fast do myelinated and unmyelinated axons conduct?

A

Myelinated - 120m/sec

Unmyelinated - 2m/sec

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16
Q

What are the 2 types of synapses and briefly explain each type

A

1) Electrical - electric current passes directly from pre to post synaptic neuron through gap junction
2) Chemical - chemical signal eg neurotransmitter

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17
Q

What are gap junctions and that are they composed of?

A
  • Intercellular channels formed by the docking of 2 hemichannels
  • Hemichannels composed of 6 connexins or innexin proteins
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18
Q

What are the 4 stages of chemical transmission?

A

1) Neurotransmitter release
2) Storage/Release
3) Receptor binding
4) Inactivation

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19
Q

What are the 3 types of classical neurotransmitters and give examples

A

1) Acetylcholine (ACH)
2) Biogenic amines
- noradrenline
- dopamine
- serotonin
- histamine
3) Amino acids
- glutamate
- gamma-aminobutyric acid (GABA)
- glycine

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20
Q

What are the 2 types of peptide neurotransmitters

A
  • Substance P

- Opioids (endorphins, enkephalins)

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21
Q

What are the 3 types of unconventional transmitters and give examples

A

Gases: nitric oxide
Purines: adenosine triphosphate (ATP)
Lipids: cannabinoids

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22
Q

How are neurons named?

A

Neurotransmitter + ‘ergic’
e.g cholinergic neurons secrete ACH
noradrenergic secrete noradrenaline

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23
Q

Explain how ACH is synthesised?

A
  • synthesised in the nerve terminal
  • choline taken from plasma
  • acetyl-CoA derived from glucose metabolism in mitochondria
  • choline acetyltransferase catalyses transfer of acetyl group from acetyl-CoA to make acetylcholine
  • Vesicular acetylcholine transporter (VACHT) loads acetylcholine into vesicles
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24
Q

Explain how ACH is degraded

A
  • Degraded by acetylcholinesterase found in extracellular space and postsynaptic membrane
  • Broken down into acetic acid and choline
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25
Q

What are constitutive and regulated exocytosis?

A

Constitutive - constant flow of material out of the membrane

Regulated - material only moved when triggered by other factor

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26
Q

Outline the mechanism of neurotransmitter release

A

11) Action potential depolarises the nerve terminal
2) Voltage gated Ca2+ channels open
Ca2+ moves into presynaptic cell by diffusion
3) Ca2+ binds to regulatory proteins on synaptic vesicle membrane and triggers the vesicle to fuse with the PM, releasing neurotransmitter
4) Neurotransmitter binds to receptors on post synaptic membrane, exciting or inhibiting the post synaptic cell

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27
Q

What are the 2 main types of neurotransmitter receptors?

A

1) Ionotrophic - transmitter binding opens an ion cchannel

2) Metabotrophic/G protein coupled - transmitter binding changes concentration of intracellular metabolites e.g CAMP

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28
Q

By what 2 methods are neurotrasmitters removed from the synaptic cleft?

A

1) Enzyme degradation in synaptic cleft

2) Re-uptake into nerve terminal or glia followed by enzyme metabolism

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29
Q

How are ACH, biogenic amines and amino acids removed?

A
  • ACH broken down by acetylcholinesterase in synaptic cleft
  • Biogenic amines taken into nerve terminal
  • Amino acids taken into nerve terminal and glia
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30
Q

What are the outermost protective layers of the CNS and what are their structures?

A

Cranium and vertebral column

  • Cranial bones interconnected by immovable fibrous joints
  • Vertebrae (7 cervical, 12 thoracic, 5 lumbar, 5 fused sacral and 4 fused coccyx) separated by intervertebral disks that permit limited movement
  • nerves of the PNS enter and leave spinal cord through spaces in stacked vertebrae
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31
Q

What protects the CNS between the bone and the nerves?

A

Meninges

  • protective membranes between the bone and the nervous tissue
  • Dura mater: outer, next to bone
  • Arachnoid membrane: middle
  • Pia matar: inner, next to nerves
  • subarachnoid space between arachnoid membrane and pia mater contains cerebrospinal fluid (CSF)
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32
Q

What is the total volume of the fluid compartments of the brain and what does it consist of?

A

Internal volume of cranium ~ 1.4 L = 1L cells and 0.4L fluid

  • 100-150ml blood
  • cerebrospinal fluid: in brain ventricles and subarachnoid space
  • interstitial fluid: inside pia matar
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33
Q

What are the characteristics of CSF

A
  • produced by the choroid plexus
  • filtrate of blood that contains no blood cells, vvery little protein and different ionic composition (similar Na+, less K+, Ca2+, HCO-)
  • absorbed back into blood by villi on arachnoid membrane
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34
Q

What are the characteristics of the choroid plexus

A
  • lines the ventricles
  • consists of transporting epithelia and capillaries
  • filters blood, removing cells, most protein and some other solutes
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35
Q

Why is the blood brain barrier necessary?

A
  • 15% of the total blood pumped from heart (1L/min) goes to the brain
  • Neurons require high oxygen levels and glucose to make ATP for active transport BUT must be protected from toxins and harmful substances
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36
Q

Describe the structure of the blood-brain barrier

A
  • Specialised selectively permeable capillaries
  • Capillary endothelial cells have tight junctions and use membrane transporters to move nutrients from blood to brain
  • Astrocyte foot processes surround the capillaries and secrete molecules that induce tight junction formation
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37
Q

What are the 3 main regions of the CNS

A

1) Cerebrum - large, folded
2) Cerebellum - second largest region of brain, sits under cerebrum
3) Brain stem and spinal cord

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38
Q

Test on brain regions and diagram in notes

A

.

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39
Q

Describe the ascending and descending tracts of the spinal cord

A

Ascending - sensory info from spinal cord to brain

Descending - motor info from brain to spinal cord

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40
Q

Where do sensory neurons enter the SC and motor neurons leave the SC

A

Sensory neurons - have cell bodies in dorsal root ganglion, enter the dorsal side of the SC
Motor neurons - have cell bodies in the ventral horn, leave the SC in the ventral root

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41
Q

What are the 2 types of efferent neurons?

A

1) Somatic motor: to skeletal muscle to control posture and movement
2) Autonomic: innervate smooth and cardiac muscle

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42
Q

What neurotransmitter and receptor is used in the somatic motor pathway?

A

ACH and nicotinic ACH receptor

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43
Q

What is a motor unit?

A

a motor neuron and all the muscle fibres it innervates

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44
Q

Where do sympathetic and parasympathetic neurons originate from?

A

Sympathetic - thoracic and lumbar regions of SC

Parasympathetic - brain stem or sacral region of the SC

45
Q

For the sympathetic nervous system, what neurotransmitter and receptor is used for both the pre and postganglionic neuron.

A

Pre: ACH and nicotinic ACH receptor
Post: Noradrenaline and adrenergic receptor

46
Q

For the parasympathetic nervous system, what neurotransmitter and receptor is used for both the pre and postganglionic neuron.

A

Pre: ACH and nicotinic ACH receptor
Post: ACH and muscarinic ACH receptor

47
Q

Describe the structure of nerve terminals that innervate smooth muscle

A

Axons end with a series of varicosities, each containing synaptic vesicles
Neurotransmitter released diffusely over the muscle fibres

48
Q

What are the main 2 neurodegenerative diseases

A

Alzheimer’s disease

Parkinson’s disease

49
Q

What are the 3 main demyelinating diseases?

A

Multiple sclerosis
Guillain-Barré syndrome
Charcot-Marie-Tooth Disease

50
Q

What are the 2 main disorders of neurotransmitter systems?

A

Myasthenic disorders: neuromuscular junction

Depression

51
Q

When was alzheimer’s first described?

A

1907

52
Q

How much of the world population is affected by Alzheimer’s and how many people is this

A

~0.5% of the worlds population

~ 35 million people

53
Q

What % of people over 65 and 80 have Alzheimer’s?

A

over 65: 7-10%

over 80: 40%

54
Q

What are the symptoms of Alzheimer’s disease?

A

Cognitive impairment:

  • Loss of memory
  • Inability to communicate
55
Q

What causes Alzheimer’s

A

Degeneration of cholinergic neurons of the forebrain

56
Q

What does the brain of an Alzheimer’s patient look like?

A

Surface of brain shows enlarged sulci (grooves) and reduced gyri (folds) due to neuronal loss

57
Q

What are amyloid plaques?

A

extracellular deposits of degenerating nerve processes and a core of insoluble beta-amyloid protein

58
Q

What are Neurofibrillary tangles?

A

NFTs are found in neuronal cell bodies and axons and are composed of a hyperphosphorylated form of the microtubule associated protein tau that aggregates into paired helical filament

59
Q

What are the genetic factors that cause Alzheimer’s?

A

Mutations in the genes encoding amyloid precursor protein (APP) and presenilin among others

60
Q

What is the environmental factor thought to contribute to Alzheimer’s disease?

A

high soil levels of aluminium

61
Q

How do APP and Presenilin mutations lead to formation of amyloid plaques?

A
  • Amyloid precursor protein is a membrane protein normally found in neurons
  • Secretase enzymes (alpha, beta and gamma secretase) cleave APP into fragments
  • Presenilin is necessary for gamma-secretase activity
  • Some fragments such as p3 are harmless
  • AB fragments, particularly AB42, are toxic to neurons
  • Amount of toxic AB42 increases when APP or presenilin are mutated
62
Q

What is the only current treatment for Alzheimer’s?

A

Acetylcholinesterase inhibitors or ACH receptor agonists that mimic ACH alleviate symptoms in some patients

63
Q

What are the 4 possible future treatments for Alzheimer’s?

A
  • Secretase inhibitors to prevent formation of amyloid plaques or agents to dissolve plaques
  • Antibody based drugs designed to target toxic AB
  • Vaccine to improve immunity to toxic AB
  • Stem cells to replace lost neurons
63
Q

When was Parkinson’s first described?

A

1817

64
Q

What % of the worlds population is affected by Parkinson’s?

A

0.2%

65
Q

What are the symptoms of Parkinson’s?

A

Tremor of the limbs
Difficulty initiating movement
Abnormal gait-walking like a shuffling run (“festination”)
Jerky movements due to rigidity around joints (“cogwheeling”)

66
Q

What is Parkinson’s caused by?

A

Degeneration in dopaminergic neurons of the nigrostriatal pathway that controls movement

67
Q

What is the nigrostiatal pathway?

A

Neurons that project from the substantia nigra to the striatum

68
Q

What causes dopaminergic neurons to degenerate?

A

dense deposits called Lewy bodies

69
Q

What environmental factors cause Parkinson’s?

A
  • MPTP is oxidised by the enzyme monoamine oxidase found in dopaminergic neurons and in glia, to MPP+ which inhibits mitochondria function killing the cell
  • Exposure to pyridine compounds in herbicides and pesticides may cause or increase the risk of Parkinson’s
70
Q

What 2 gene mutations cause Parkinson’s?

A

1) SNCA gene that encodes the protein alpha-synuclein
2) PARK2 gene that encodes the protein parkin

  • Alpha-synuclein is a nerve terminal protein
  • Parkin is an enzyme component of the ubiquitin-proteasome pathway responsible for removal of damaged or excess protein
  • Gene mutations lead to Lewy Bodies, the main component of which is a toxic form of alpha-synuclein
71
Q

What are the 2 main current treatments for Parkinson’s and give examples for each

A

1) Drugs
- L-DOPA, the precursor of dopamine, acts to restore brain dopamine levels
- Inhibitors of enzyme monoamine oxidase which degrades dopamine

2) Deep brain stimulation
- surgical procedure; electrodes implanted to override the abnormal electrical impulses

72
Q

Name a potential future treatment

A

Cell replacement by stem cells

73
Q

What % of the population suffer from MS?

A

~0.04%

- Over 1% in Northern Europe, North America, Australia and New Zealand

74
Q

When does diagnosis usually occur?

A

Between 20-40

75
Q

What causes MS?

A

Lesions, progressing to sclerosis, form in the myelin sheath of the CNS, leading to inflammation and loss of myelin

76
Q

What are some symptoms of MS?

A

Difficulty walking
Visual problems
Fatigue

77
Q

Name the 4 types of MS and give a description of each

A

1) Relapsing Remitting MS (RRMS)
- ~80% of patients in early phase of disease
- altering periods of illness and recovery, no marked degradation over time

2) Secondary Progressive MS (SPMS)
- high % of RRMS patients develop SPMS ~10 years after onset
- Progressive neurological deterioration, fewer remissions, incomplete recovery

3) Progressive Relapsing MS (PRMS)
- ~5% of patients
- alternating periods of relapse and remission but progressive deterioration between relapses

4) Primary Progressive (PPMS)
~ 10-15% of patients
- progressive from onset - no remissions

78
Q

Other than genetics, what other 2 reasons are suggested for causing MS?

A

1) Infectious agent
- Focus on Epstein Barr but others too e.g measles, herpes, chlamydia

2) Immune-mediated
- Antibodies produced attack myelin sheath
- May involve molecular mimicry - normal protein resembles foreign substance so is attacked

79
Q

What gene complex is associated with contributing to MS?

A

Major histocompatibility complex (MHC)

80
Q

Name the 4 methods used to diagnose MS

A
  • ‘Hot bath test’ - raising body temp slows conduction in demyelinated plaques, amplifying symptoms
  • Nerve conduction test
  • Sampling of CSF by lumbar puncture for presence of white blood cells or antibodies
  • MRI to look for abnormalities in white matter
81
Q

What are the 2 treatments for MS?

A
  • Drugs such as beta-interferons

- Exercise, physio, diet

82
Q

What is Guillian-Barre Syndrome and when was it first described

A
  • Autoimmune demyelinating disease

- 1916

83
Q

What is the prevalence of this disease?

A

1-2 in 100,000

84
Q

What are the symptoms of the disease and which neurons cause each one?

A

General peripheral neuropathy affecting:

  • somatic motor neurons (paralysis, respiratory problems)
  • sensory neurons (loss of sensation)
  • autonomic neurons (fluctuating blood pressure, cardiac arrhythmia’s)
85
Q

What causes GB syndrome?

A

Antibodies, triggered by viral infection or immunisation, attack components of Schwaan cell myelin

86
Q

What are the 2 treatments for GB syndrome?

A
  • Immunoglobulins administered intravenously

- Plasmapheresis (plasma exchange)

87
Q

What is Charcot-Marie-Tooth Disease (CMT) and when was it first described?

A
  • Inherited demyelinating disease

- 1880s

88
Q

What are the symptoms of CMT disease?

A

Peripheral motor and sensory neuropathy

  • weakness of leg, foot and hand muscles (motor)
  • reduced ability to perceive pain, temp etc (sensory)
89
Q

How common is CMT disease?

A

1 in 2500

90
Q

How is CMT disease inherited?

A
  • ~ 80-90% is autosomal (dominant or recessive)

- remainder are X linked (CMTX)

91
Q

What is Connexin 32 and what is its role in CMT disease?

A
  • Found in Schwaan cells and forms gap junctions between layers of myelin membranes surrounding peripheral axons
  • Gap junctions provide route for transfer of nutrients through the myelin to inner myelin layers
  • Cx332 loff of function mutations lead to degredation of inner myelin and the axon
92
Q

What are the symptoms of Myasthenic disorders?

A
  • Muscular weakness

- Fatigability affecting ocular, facial, respiratory and limb muscles

93
Q

Are myasthenic disorders autoimmune or genetic?

A

Both

94
Q

What is the prevalence of Myasthenia Gravis?

A

15-20 in 100,000

95
Q

What causes Myasthenia Gravis?

A

Auto antibodies attack protein subunits of the nicotinic ACH receptor
- antibodies either block transmitter binding, increase rate of receptor degradation or destroy post synaptic membrane resulting in cell lysis

96
Q

What causes Lambert-Eaton Myathenia (LEMs)

A
  • auto antibodies attack voltage gated Ca2+ channels in the motor neuron presynaptic terminal, reducing ACH release

(may be associated with lung or other cancers)

97
Q

What causes Congenital Myasthenia Syndromes (CMS)?

A

mutations in gene for nicotinic ACH receptor subunits causing ACH receptor deficiency

98
Q

What causes Congenital Myasthenia Syndrome with Episodic Apnea (CMSEA)

A
  • mutations in choline acetyltransferase, less ACH produced
99
Q

What causes End Plate Acetylcholinesterase Deficiency?

A

Mutations in acetylcholinesterase, overstimulation of skeletal muscle

100
Q

What % of the worlds population suffer from depression?

A

10%

101
Q

What are some symptoms of depression?

A
  • Alterations in mood
  • Inability to sleep
  • Changes in appetite
102
Q

What is Endogenous Depression?

A
  • Arises without any identifiable cause

- Very likely to have a genetic basis

103
Q

What is Exogenous Depression?

A
  • Associated with a stressful lifestyle
104
Q

What are the 2 subdivisions of both endogenous and exogenous depression?

A
  • Monopolar (major depression) and Bipolar (manic depression)
105
Q

What happens to neurotransmitters during depression?

A
  • Associated with imbalances in activity of central monoaminergic and cholinergic pathways of limbic system
  • lower than normal activity at synapses using monoamine transmitters; noradrenaline, dopamine and serotonin
  • relative over activity at cholinergic synapses
106
Q

Is depression a single gene or multiple gene disorder?

A

Multiple

107
Q

What is the major treatment for depression and give examples

A

Drug treatments aim to elevate levels of monoamine transmitters at the synapse:

  • tricyclic antidepressants (eg amitriptyline) block reuptake of noradrenaline
  • selective seretonin reuptake inhibitors (SSRI’s eg Prozac/Fluoxetine)
  • monoamine oxidase (MAO) inhibitors prevent breakdown of monoamine transmitters

Biomed (18 decks)

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